Tuesday, June 19, 2007

Hypersexual sensations and behavior in a multiple sclerosis exacerbation: a case report

C C Yang1, B Severson2 and J D Bowen3

1Department of Urology, University of Washington, Seattle, Washington, USA

2Department of Physical Medicine and Rehabilitation, University of Washington, Seattle, Washington, USA

3Department of Neurology, University of Washington, Seattle, Washington, USA

Correspondence to: CC Yang, Department of Urology, Box 356510, University of Washington, Seattle, WA 98195-6510, USA. E-mail: cyang@u.washington.edu

International Journal of Impotence Research (2004) 16, 382-384. doi:10.1038/sj.ijir.3901201
Published online 11 March 2004

Keywords

multiple sclerosis; female sexual function; hypersexuality

Introduction

Hypersexual sensations and behavior are documented in a variety of neurologic disorders, including head trauma,1 Kluver Bucy syndrome,2 following neurosurgical procedures,3, 4 Parkinson's disease,5 and stroke.6 However, hypersexuality associated with multiple sclerosis (MS) is rare.7 The typical manifestation of a sexual dysfunction in MS is loss of libido, sexual arousal, or orgasmic capacity.8, 9, 10 We report on a woman with MS who experienced hypersexual feelings and behavior as part of an MS exacerbation.

Case report

A 51-year-old female elementary teacher with MS presented with a complaint of sudden onset increased libido and sexual activity. 10 days prior to this, she awoke, from a 'gunshot'-type sound in her head. It was immediately followed by two other similar sounds, localized to above her left ear. Following these events, the patient's sexual appetite became insatiable. She was happily married for 25 y, reported a healthy sex life, but this behavior was completely atypical. After a few days of frequent intercourse, her husband was unable to keep up with her requests for sex. She masturbated frequently to relieve her sexual desire, and had never done so previously. Masturbation did not always result in orgasm, and it was generally not satisfying.

The patient experienced a concurrent increase in generalized body hypersensitivity, breast tenderness and engorgement, and genital arousal, with and without sexual stimulation. Wearing a bra became uncomfortable, and movement of her pelvis (eg, while riding in a car) increased her genital arousal almost to the point of orgasm. Her sexual responsiveness increased significantly. She had mild urge incontinence due to her MS, but during this episode became more continent of urine and had increased constipation.

She also experienced more behavioral impulsiveness. For the first time, she began swearing at her husband, and bought $200 worth of lottery tickets, having never before gambled in her life.

The patient's sexual changes became a significant source of stress. She felt shameful, and worried about self-control in the presence of other men, even contemplating marital infidelity to satisfy her sexual urges. She had a history of depression with the onset of MS, but denied mania or psychotic symptoms. She was not on any antidepressants, but was under the care of a psychologist.

Her MS was diagnosed 9 y prior, and was the relapsing-remitting type. Her functional status was still very high, and her primary symptoms due to MS were fatigue and slight difficulty with balance. She had undergone a hysterectomy and bilateral oophorectomy 20 y prior for benign disease. Her medications included gabapentin 800 mg qd, IFN beta 1-B (Betaseron) 8 million IU S.C. q.o.d., rofecoxib p.r.n., modafinil 200 mg q a.m., estradiol 5 mg i.m. once per week, and estrogen vaginal cream p.r.n.

Her neurological examination was essentially unchanged from previous visits. Remarkable findings included decreased pinprick left cheek, diminished motor strength 4/5 left dorsiflexion, knee extension, and hip flexion, unsteady gait with an inability to perform heel, toe, or tandem gaits.

Her external female genitalia was mildly atrophic. The vaginal mucosa was healthy, but dry; the urethral meatus was normal. She had impaired sensation to light touch and pinprick on both her labia and perianal areas. Sensation to bimanual examination was mildly diminished. A bulbocavernosus reflex was absent. Her pelvic floor contraction strength was poor.

She completed the Female Sexual Function Index (FSFI),11 a validated measure of female sexual functioning. She rated her sexual functioning at 33.3 out of a possible 36. The domain with the most significant dysfunction was in sexual satisfaction.

A brain MRI with gadolinium demonstrated multiple periventricular white matter lesions consistent with MS, which was stable from previous studies (Figure 1). Estrogen, progesterone, total testosterone, FSH, LH levels were normal, and an estradiol level was elevated at 717 pg/ml. Urinalysis, CBC, comprehensive metabolic panel, and TSH were normal.

Because of the acuity of the episode and the constellation of symptoms, this change in sexual behavior was considered to be part of an MS exacerbation. She received methoprednisolone 1 g i.v. for 5 days, followed by an oral prednisone taper. This resulted in an immediate reduction in all of her symptoms. A few days after the steroid pulse, her symptoms returned, but with less intensity than the original episode. A repeat brain MRI with gadolinium was unchanged. A second 5-day course of i.v. methylprednisolone was given, resulting in complete resolution of all of her symptoms. Her FSFI score dropped to 28.4, with the domain of sexual desire score dropping dramatically.

Discussion

Hypersexual behavior is rare in MS. Its acute onset and resolution with steroids in this case suggested that it was due to an MS exacerbation. Although there was no radiographic change suggesting an increase in plaque load, there are many studies documenting the lack of association between symptoms and MRI findings.12

Other causes of hypersexuality are unlikely in this case. MRI did not identify any other central nervous system lesions other than the pre-existing periventricular MS plaques. Hormonal changes are unlikely as she had been on a stable replacement regimen of estrogen for 20 y, following gynecologic surgery. Her replacement frequency was cut in half during the second exacerbation to minimize the possibility of the hormones exacerbating her problems, but it was not discontinued as that would have likely worsened her emotional lability. Furthermore, the acute changes in impulsivity, disinhibition, and personality are unlikely to be explained by hormonal change, and are more likely to be a result of a frontal lobe lesion. The patient had been on modafinil for 16 months, and thus this medication would not have been related to the patient's symptoms. Primary psychiatric conditions would not be expected to improve with corticosteroids. This symptom complex is not a result of a lumbosacral spinal lesion because there were no manifestations of lower motor neuron functional loss, which would have been the case with a lesion in that area. Sacral MS plaques typically manifest as loss of bladder, bowel, or sexual function, not improved function.13

From a neuroanatomic standpoint, this case may represent an example of increased sexual desire and responsiveness associated with a frontal lobe lesion. The disinhibition resulted in increased impulsiveness as well as hypersexual behavior. However, this is all speculative as there were no new identifiable lesions on brain MRI that appeared since her previous studies.

References

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12 Kappos L et al. Predictive value of gadolinium-enhanced magnetic resonance imaging for relapse rate and changes in disability or impairment in multiple sclerosis: a meta-analysis. Gadolinium MRI Meta-analysis Group. Lancet 1999; 353: 964-969. Article PubMed

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Figures

Figure 1 MRI showing multiple periventricular white matter lesions on T2 imaging, consistent with multiple sclerosis.

Received 23 September 2003; revised 8 December 2003; accepted 26 January 2004; published online 11 March 2004

August 2004, Volume 16, Number 4, Pages 382-384

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